Michael P. D'Alessandro, M.D.
Peer Review Status: Internally Peer Reviewed
Normal fetuses have rapid and shallow respiratory movements in utero. If a fetus becomes distressed and hypoxemic these rapid movements cease. If hypoxia persists the fetal apnea is replaced by deep gasping respiratory movements. The fetal lung fluid is replaced by aspirated amniotic fluid which contains meconium because fetal hypoxia can also stimulate colonic contraction and evacuation of meconium into the amniotic fluid. The pulmonary problems therefore are due to a combination of aspirated meconium causing mechanical obstruction of the major airways and a more peripheral chemical pneumonitis. If obstruction is complete, death occurs. Much more likely is partial airway obstruction with peripheral air trapping, often leading to air leak complications. Longer term, exposure of the smaller airways and alveoli to the necrotizing effects of meconium can result in chemical pneumonitis with alveolar collapse and cellular necrosis. This results in increased airway reactivity and a generalized obstructive phenomenon that usually resolves slowly during the first year of life. Treatment is optimized to clear the aspirated amniotic fluid and meconium by immediate postnatal suctioning before the meconium disseminates peripherally.
Meconium throughout the airways causing chemical pneumonitis with alveolar collapse and necrosis.
Increased lung volume and irregular aeration with coarse, patchy densities representing scattered areas of atelectasis and consolidation mixed with focal areas of overinflation and peripheral air trapping. Air leak and pneumomediastinum/pneumothorax is common. Pleural effusions are often present.
See References Chapter.
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